CoChat
Sign Up
Cited by 38

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Activation-Induced Cytidine Deaminase Accelerates Clonal Evolution in BCR-ABL1 –Driven B-Cell Lineage Acute Lymphoblastic Leukemia

Gruber, Tanja Andrea, Chang, Mi Sook, Sposto, Richard, Müschen, Markus·2010·Cancer Research
DOI 10.1158/0008-5472.can-10-1438PMC PMC2948648

Published version of a preprint

Open this paper in CoChat — free account

Abstract

Activation-induced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center (GC) B cells. Occasionally, AID can target non-Ig genes and thereby promote GC B-cell lymphomagenesis. We recently showed that the oncogenic BCR-ABL1 kinase induces aberrant expression of AID in pre-B acute lymphoblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis. To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL. Mice transplanted with BCR-ABL1–transduced AID−/− bone marrow had prolonged survival compared with mice transplanted with leukemia cells generated from AID+/+ bone marrow. Consistent with a causative role of AID in genetic instability, AID−/− leukemia had a lower frequency of amplifications and deletions and a lower frequency of mutations in non-Ig genes, including Pax5 and Rhoh compared with AID+/+ leukemias. AID−/− and AID+/+ ALL cells showed a markedly distinct gene expression pattern, and AID−/− ALL cells failed to downregulate a number of tumor-suppressor genes including Rhoh, Cdkn1a (p21), and Blnk (SLP65). We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic instability and aberrant somatic hypermutation, and by negative regulation of tumor-suppressor genes. Cancer Res; 70(19); 7411–20. ©2010 AACR.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1158/0008-5472.can-10-1438

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 2 references

Research works printed but not linked: 46

  1. Muramatsu, 2000, Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme, Cell, 102, 553, 10.1016/S0092-8674(00)00078-7 · DOI
  2. Revy, 2000, Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2), Cell, 102, 565, 10.1016/S0092-8674(00)00079-9 · DOI
  3. Ramiro, 2007, The role of activation-induced deaminase in antibody diversification and chromosome translocations, Adv Immunol, 94, 75, 10.1016/S0065-2776(06)94003-6 · DOI
  4. Liu, 2008, Two levels of protection for the B cell genome during somatic hypermutation, Nature, 451, 841, 10.1038/nature06547 · DOI
  5. Pasqualucci, 2001, Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas, Nature, 412, 341, 10.1038/35085588 · DOI · Paper page
  6. Neuberger, 1998, Monitoring and interpreting the intrinsic features of somatic hypermutation, Immunol Rev, 162, 107, 10.1111/j.1600-065X.1998.tb01434.x · DOI
  7. Pasqualucci, 2008, AID is required for germinal center-derived lymphomagenesis, Nat Genet, 40, 108, 10.1038/ng.2007.35 · DOI
  8. Robbiani, 2008, AID is required for chromosomal breaks in c-myc that lead to c-myc/IgH translocations, Cell, 135, 1028, 10.1016/j.cell.2008.09.062 · DOI
  9. Tsai, 2008, Human chromosomal translocations at CpG sites and a theoretical basis for their lineage and stage specificity, Cell, 135, 1130, 10.1016/j.cell.2008.10.035 · DOI
  10. Pui, 2004, Acute lymphoblastic leukemia, N Engl Med, 350, 1535, 10.1056/NEJMra023001 · DOI
  11. Schultz, 2009, Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a Children's Oncology Group study, J Clin Oncol, 27, 5175, 10.1200/JCO.2008.21.2514 · DOI
  12. Feldhahn, 2007, Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells, J Exp Med, 204, 1157, 10.1084/jem.20062662 · DOI
  13. Iacobucci, Different isoforms of the B-cell mutator activation-induced cytidine deaminase are aberrantly expressed in BCR-ABL1-positive acute lymphoblastic leukemia patients, Leukemia
  14. Klemm, 2009, The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia, Cancer Cell, 16, 232, 10.1016/j.ccr.2009.07.030 · DOI
  15. Mullighan, 2008, BCR-ABL1 lymphoblastic leukemia is characterized by the deletion of Ikaros, Nature, 453, 110, 10.1038/nature06866 · DOI · Paper page
  16. Soneoka, 1995, A transient three-plasmid expression system for the production of high titer retroviral vectors, Nucleic Acids Res, 23, 628, 10.1093/nar/23.4.628 · DOI
  17. Pear, 1998, Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving p210 bcr/abl-transduced bone marrow, Blood, 92, 3780, 10.1182/blood.V92.10.3780 · DOI
  18. Dickerson, 2003, AID mediates hypermutation by deaminating single stranded DNA, J Exp Med, 197, 1291, 10.1084/jem.20030481 · DOI
  19. Chua, 2002, The function of AID in somatic mutation and class switch recombination: upstream or downstream of DNA breaks, J Exp Med, 195, F37, 10.1084/jem.20020380 · DOI
  20. Schlissel, 1993, Double-strand signal sequence breaks in V(D)J recombination are blunt, 5′-phosphorylated, RAG-dependent, and cell cycle regulated, Gene Dev, 7, 2520, 10.1101/gad.7.12b.2520 · DOI
  21. Voncken, 1992, Clonal development and karyotype evolution during leukemogenesis of BCR-ABL transgenic mice, Blood, 79, 1029, 10.1182/blood.V79.4.1029.bloodjournal7941029 · DOI
  22. Pollack, 2002, Microarray analysis reveals a major direct role of DNA copy number alteration in the transcriptional program of human breast tumors, Proc Natl Acad Sci U S A, 99, 12963, 10.1073/pnas.162471999 · DOI
  23. Jumaa, 2003, Deficiency of the adaptor SLP-65 in pre-B-cell acute lymphoblastic leukaemia, Nature, 423, 452, 10.1038/nature01608 · DOI
  24. Borkhardt, 2000, The human GRAF gene is fused to MLL in a unique t(5;11)(q31;q23) and both alleles are disrupted in three cases of myelodysplastic syndrome/acute myeloid leukemia with a deletion 5q, Proc Nat Acad Sci U S A, 97, 9168, 10.1073/pnas.150079597 · DOI
  25. Liu, 2001, RhoB is required to mediate apoptosis in neoplastically transformed cells after DNA damage, Proc Natl Acad Sci U S A, 98, 6192, 10.1073/pnas.111137198 · DOI
  26. Yang, 1995, The p21 cyclin-dependent kinase inhibitor suppresses tumorigenicity in vivo, Nat Med, 1, 1052, 10.1038/nm1095-1052 · DOI
  27. Gu, 2005, RhoH, a hematopoietic-specific Rho GTPase, regulates proliferation, survival, migration, and engraftment of hematopoietic progenitor cells, Blood, 105, 1467, 10.1182/blood-2004-04-1604 · DOI · Paper page
  28. Williams, 2008, Rho GTPases and regulation of hematopoietic stem cell localization, Method Enzymol, 439, 365, 10.1016/S0076-6879(07)00427-2 · DOI · Paper page
  29. Krause, 2006, Requirement for CD44 in homing and engraftment of BCR-ABL-expressing leukemia stem cells, Nat Med, 12, 1175, 10.1038/nm1489 · DOI · Paper page
  30. Whibley, 2009, p53 polymorphisms: cancer and implications, Nat Rev Cancer, 9, 95, 10.1038/nrc2584 · DOI
  31. Godar, 2008, Growth-inhibitory and tumor suppressive functions of p53 depend on its repression of CD44 expression, Cell, 134, 62, 10.1016/j.cell.2008.06.006 · DOI
  32. Kleijnen, 2000, The hPLIC proteins may provide a link between the ubiquitination machinery and the proteasome, Mol Cell, 6, 409, 10.1016/S1097-2765(00)00040-X · DOI
  33. Trotta, 2003, BCR/ABL activates mdm2 mRNA translation via the La antigen, Cancer Cell, 3, 145, 10.1016/S1535-6108(03)00020-5 · DOI
  34. Honda, 2000, Acquired loss of p53 induces blastic transformation in p210bcr/abl-expressing hematopoietic cells: a transgenic study for blast crisis of human CML, Blood, 95, 1144, 10.1182/blood.V95.4.1144.004k04_1144_1150 · DOI
  35. Papavasiliou, 2000, Cell-cycle-regulated DNA double-strand breaks in somatic hypermutation of immunoglobulin genes, Nature, 408, 216, 10.1038/35041599 · DOI
  36. Phan, 2004, The BCL6 proto-oncogene suppresses p53 expression in germinal-centre B cells, Nature, 432, 635, 10.1038/nature03147 · DOI
  37. Muto, 2006, Negative regulation of activation-induced cytidine deaminase in B cells, Proc Natl Acad Sci U S A, 103, 2752, 10.1073/pnas.0510970103 · DOI
  38. Ramiro, 2006, Role of genomic instability and p53 in AID-induced c-myc-Igh translocations, Nature, 440, 105, 10.1038/nature04495 · DOI
  39. Soverini, 2006, Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia, Clin Cancer Res, 12, 7374, 10.1158/1078-0432.CCR-06-1516 · DOI
  40. Hu, 2004, Requirement of Src kinases Lyn, Hck, and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia, Nat Genet, 36, 453, 10.1038/ng1343 · DOI
  41. Wu, 2008, Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase, J Natl Cancer Inst, 100, 926, 10.1093/jnci/djn188 · DOI
  42. Blake, 2000, SU6656, a selective Src family kinase inhibitor, used to probe growth factor signaling, Mol Cell Biol, 20, 9018, 10.1128/MCB.20.23.9018-9027.2000 · DOI
  43. Bhutani, 2010, Reprogramming towards pluripotency requires AID-dependent DNA demethylation, Nature, 463, 1042, 10.1038/nature08752 · DOI
  44. Popp, 2010, Genome-wide erasure of DNA methylation in mouse primordial germ cells is affected by AID deficiency, Nature, 463, 1101, 10.1038/nature08829 · DOI
  45. Muramatsu, 1999, Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells, J Biol Chem, 274, 18471, 10.1074/jbc.274.26.18470 · DOI
  46. Beumer, 2008, Concentrations of the DNA methyltransferase inhibitor 5-fluoro-2′-deoxycytidine (FdCyd) and its cytotoxic metabolites in plasma of patients treated with FdCyd and tetrahydrouridine (THU), Cancer Chemother Pharmacol, 62, 363, 10.1007/s00280-007-0603-8 · DOI

Cited by

Metadata

Authors
Gruber, T. A., Chang, M. S., Sposto, R., & Müschen, M.
Affiliations
Authors' Affiliations: 1Childrens Hospital Los Angeles and 2Department of Laboratory Medicine, University of California San Francisco, San Francisco, California
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2010-09-29
Volume
70
Issue
19
Pages
7411-7420
ISSN
  • 0008-5472
  • 1538-7445
DOI
10.1158/0008-5472.can-10-1438
PMC
PMC2948648
Cited by
38
References
2
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review